Evidence map›Paper›PMID 38918360›Full record

ArticleCell death & disease2024

IGFBP2/ITGA5 promotes gefitinib resistance via activating STAT3/CXCL1 axis in non-small cell lung cancer.

Hengxiao Lu, Jiangshan Ai, Yingying Zheng, Wolong Zhou, Liming Zhang, Jiebo Zhu, Heng Zhang, Shaoqiang Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Review
  2. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Hengxiao Lu *Department of Thoracic Surgery, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261041, Shandong Province, China.
Jiangshan Ai *Department of Thoracic Surgery, Affiliated Hospital of Qingdao University, Qingdao, 266003, Shandong Province, China.
Yingying ZhengHealth Management Center, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261041, Shandong Province, China.
Wolong ZhouDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, 87# Xiangya Road, Changsha, 410008, Hunan Province, China.
Liming ZhangDepartment of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, 272029, Shandong Province, China.
Jiebo ZhuDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, 87# Xiangya Road, Changsha, 410008, Hunan Province, China.
Heng ZhangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, 87# Xiangya Road, Changsha, 410008, Hunan Province, China. 404346@csu.edu.cn.ORCID 0000-0002-1554-2051
Shaoqiang WangDepartment of Thoracic Surgery, Weifang People's Hospital, Shandong Second Medical University, Weifang, 261041, Shandong Province, China. rmyywsq227@wfmc.edu.cn.ORCID 0000-0001-6023-8203

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is a paucity of comprehensive knowledge pertaining to the underlying mechanisms leading to gefitinib resistance in individuals diagnosed NSCLC harboring EGFR-sensitive mutations who inevitably develop resistance to gefitinib treatment within six months to one year. In our preceding investigations, we have noted a marked upregulation of IGFBP2 in the neoplastic tissues of NSCLC, predominantly in the periphery of the tissue, implying its plausible significance in NSCLC. Consequently, in the current research, we delved into the matter and ascertained the molecular mechanisms that underlie the participation of IGFBP2 in the emergence of gefitinib resistance in NSCLC cells. Firstly, the expression of IGFBP2 in the bronchoalveolar lavage fluid and lung cancer tissues of 20 NSCLC patients with gefitinib tolerance was found to be significantly higher than that of non-tolerant patients. Furthermore, in vitro and in vivo experiments demonstrated that IGFBP2 plays a significant role in the acquisition of gefitinib resistance. Mechanistically, IGFBP2 can activate STAT3 to enhance the transcriptional activity of CXCL1, thereby increasing the intracellular expression level of CXCL1, which contributes to the survival of lung cancer cells in the gefitinib environment. Additionally, we identified ITGA5 as a key player in IGFBP2-mediated gefitinib resistance, but it does not function as a membrane receptor in the process of linking IGFBP2 to intracellular signaling transduction. In conclusion, this study demonstrates the promoting role and mechanism of IGFBP2 in acquired gefitinib resistance caused by non-EGFR secondary mutations, suggesting the potential of IGFBP2 as a biomarker for gefitinib resistance and a potential intervention target.

Indexed as

Carcinoma, Non-Small-Cell LungChemokine CXCL1Drug Resistance, NeoplasmGefitinibInsulin-Like Growth Factor Binding Protein 2Lung NeoplasmsSTAT3 Transcription FactorAnimalsAntineoplastic AgentsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansIntegrinsMaleMiceAntineoplastic AgentsChemokine CXCL1GefitinibIGFBP2 protein, humanInsulin-Like Growth Factor Binding Protein 2IntegrinsITGA5 protein, humanSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID38918360
PMCPMC11199710

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.